Pacemakers and implantable cardioverters/defibrillators are widely used to treat a number of different cardiac conditions. For example, localized pacing has been used to terminate and/or control bradycardia, bradyarrhythmia, tachycardia, tachyarrhythmia, and other conditions. Over the years, many sophisticated algorithms and complex electromechanical devices have been developed and implemented in pacemaker technology for detecting the onset of abnormal rhythms and treating these conditions.
To better understand the effect of pacing devices, it is useful to understand the electrical-mechanical operation of the heart. The normal electrical activation system of the heart initiates left and right heart conduction using a complex structure/network of cardiac cells that rapidly conduct cellular-level electrical activation through cardiac tissue. For example, in the left and right ventricles of the heart, the Purkinje system, a specialized network of cells, conducts electrical activation endocardially and spreads the activation through the myocardial layers to the epicardium. Via connection to the atrial-ventricular node (A-V node), which is a specialized network of cells between the atria and the ventricles, normal ventricular electrical activation originates in the superior, septal aspect of the left ventricle, and then propagates through the septal wall, left ventricular free wall, and right ventricular free wall. This electrical activation induces the mechanical contractions of the ventricles that eject blood from the heart and into the vascular system. The strength and pattern of the mechanical contractility of the heart significantly affects the hemodynamic function. For example, when the normal electrical conduction pattern is blocked by ischemic regions in the ventricles, the mechanical contraction patterns of the heart are modified. Therefore, changes in the electrical conduction pattern have a direct impact on the hemodynamic function of the heart.
In the presence of cardiac disease, the dynamic and complex changes in regional electrical conduction and in mechanical function can lead to inefficiencies and cardiac hemodynamic output that eventually cause cardiomyopathy, mitral valve regurgitation, and other global physical and functional changes. Such mechanical dysfunction leads to further electrical conduction abnormalities, and thus further mechanical dysfunction. This progressively deleterious cycle of events leads to further inefficiencies and ever-worsening cardiovascular status (e.g., progressive heart failure).
Typical pacing devices artificially initiate electrical conduction in the heart by delivering small amounts of electrical current (e.g., a stimulation pulse) between two electrical contacts (electrodes) located on a lead placed in or on the heart. At least one electrode typically touches cardiac tissue. The site of the electrical contact then becomes the earliest site of activation and a conduction pattern propagates from this site throughout the cardiac tissue. It is desirable for pacing devices to deliver the stimulation pulse to a selected site along the normal electrical conduction paths in order to more appropriately synchronize the activation pattern of the heart. In many applications, for example, it would be desirable to stimulate from an endocardial location in the left ventricle to more closely approximate the normal electrical activation that initiates in the superior, septal aspect of the left ventricle. However, as explained below, many lead-based systems cause an abnormal conduction pattern to propagate through the cardiac tissue because lead-based electrodes are limited to being placed at an abnormal site of origin.
One drawback of lead-based pacing systems is that they are not well suited for endocardial pacing in the left ventricle. For the emerging treatment of heart failure, through what is commonly known as resynchronization therapy, bi-ventricular pacing is utilized. Bi-ventricular pacing requires that an additional lead be placed in contact with the left ventricle. To access the left ventricle, a third lead is typically advanced through the right atrium and the orifice of the coronary sinus, and then the third lead is maneuvered through the coronary veins to a position in the vein that is on the epicardial aspect of the lateral wall of the left ventricle. Less commonly, the third lead is placed directly on the epicardium and then subcutaneously tunneled to the implant location of the pacing device. The left ventricle is accordingly stimulated epicardially from this position. Unlike normal endocardial electrical activation in which the activation initiates in the endocardium and then propagates through the myocardial layers to the epicardium, such epicardial stimulation of lead-based electrodes progresses in the opposite transmural direction. This approach may reduce the efficacy of lead-based left ventricular pacing. Moreover, because the size and course of the coronary sinus varies from patient to patient, it is often difficult to manipulate the lead within the coronary sinus. The available stimulation sites within the coronary sinus are accordingly limited by the individual anatomic features of each patient. Also, because the lead is located on the epicardial side of the left ventricle, the electrical current/energy required to stimulate the left ventricle is generally significantly higher for this treatment compared to standard endocardial locations within the right ventricle. This occurs, in part, because the electrical contacts of the lead may not be in intimate contact with the myocardium (i.e., they may be more preferentially in contact with the vein or situated centrally within the vessel). Thus, higher electrical currents in the stimulation pulse may be required to initiate activation. These higher electrical currents may stimulate other unintended, nearby structures such as the phrenic nerve.
Although implanting pacemaker leads directly within the left ventricle has been proposed, it is not yet practiced because prior art medical devices that reside on the arterial side (left side) of the cardiovascular system increase the risk of stroke, myocardial infarction, and vascular occlusions. For example, left ventricular lead placement is not practical because thrombus formation on the lead body and subsequent systemic embolization would require patients to have long-term anticoagulation drugs. Moreover, it may be necessary to extract the lead from the left ventricle, but this procedure may have considerable risks. Placing the lead retrograde through the aortic valve may cause aortic regurgitation and the proximate end of the lead may cause arterial bleeding because this end of the lead would need to exit through an artery. Alternatively, placing the lead through a transeptal atrial puncture and then across the mitral valve into the left ventricle, may possibly worsen mitral valve regurgitation. Therefore, implanting lead-based electrodes into the left ventricle of the patient is not practical using conventional systems.
Another aspect of implanting pacing systems is to determine the stimulation site to effectuate optimal synchronization timing between pacing sites and the resultant hemodynamic performance. Clinical studies of pacing modalities to treat heart failure have shown that acute hemodynamic measurements are correlated with patient benefit. For example, a separate catheter placed acutely within the left ventricle has been used to evaluate hemodynamic responses for bi-ventricular pacing. Specifically, a pressure-volume catheter system has been used to obtain simultaneous measurement of (a) aortic and left ventricular pressures, (b) an index of contractility (dP/dTmax), and/or (c) left ventricular chamber volumes. Based on these clinical studies, it appears that it would be desirable to optimize the number and location of the stimulation sites to provide the optimal patient benefit.
One drawback of using hemodynamic measurements within the left ventricle for pacing applications is that it is impractical to implant lead-based electrodes in the left ventricle for the reasons explained above. Therefore, even though hemodynamic responses have been evaluated for bi-ventricular pacing using epicaridal lead placements, this concept has not been used for endocardial pacing in the left ventricle because conventional pacing devices are not well suited for left ventricular pacing even if such left ventricular sites are the optimal stimulation sites.